败血症性休克现称为感染性休克,因为临床上感染性休克引起脏器功能衰竭的机制,主要是某些化学介质激活的结果。本文就感染性休克有关介质及其并发的脏器功能障碍,特别是以肺的障碍为中心,略予介绍。一、炎症的出现与扩大炎症是一种生体防御反应,这种反应受各种化学介质左右。首先是单核细胞及局部组织细胞为主的巨噬细胞被病原菌激活,释放出细胞激肽,如肿瘤坏死因子(TNF)、白细胞介素(IL-1)等。炎症初期,介质也作用于血管内皮细胞,使血管通透性增强,血浆渗出量增加,激活了体液中的抗体和补体,促进嗜中性细胞、巨噬细胞的吞噬作用。吞噬后的处理则与贮存在细胞内的溶菌酶和产生的氧游离基有关。吞噬后的细胞释放出:①氧游离基;②花生四烯酸生成的前列腺素类(PGs)、白细胞三烯类(LTs)、血小 Septic shock is now called septic shock because of the mechanism by which septic shock causes organ failure in the clinic, mainly as a result of the activation of certain chemical mediators. This article on septic shock and its associated media and organ dysfunction, especially in the lung as the center of the disorder, slightly introduced. First, the emergence of inflammation and expansion of inflammation is a biological defense response, this reaction by a variety of chemical mediators around. First of all, monocytes and local tissue-dominant macrophages are activated by pathogens and release cytokines such as tumor necrosis factor (TNF) and interleukin-1 (IL-1). In the early stages of inflammation, the mediators also act on the vascular endothelial cells, resulting in increased vascular permeability and increased plasma exudation, activating antibodies and complement in body fluids and promoting phagocytosis of neutrophils and macrophages. Post-phagocytosis treatment is associated with lysozyme stored in the cell and oxygen free radicals produced. Phagocytic cells release: ① oxygen free radicals; ② arachidonic acid generated prostaglandins (PGs), leukotrienes (LTs), small blood